Aetiology
One study that used data from a large US national claims database found that most cases of gastroparesis are due to the following aetiologies:[9]
Diabetes mellitus (57.4%; type 1, 5.7% and type 2, 51.7%)
Post-surgical complications from partial gastric resection or vagotomy, post-bariatric surgery, Nissen fundoplication, and lung or heart-lung transplantation (15%)
Drug-associated, e.g., opioids, tricyclic antidepressants, calcium-channel blockers, clonidine, dopamine agonists, lithium, nicotine, and progesterone (11.8%)
Idiopathic (11.3%).
Other less common causes include:
Gastrointestinal disorders associated with delayed gastric emptying (e.g., post-infectious gastroparesis, achalasia, atrophic gastritis, functional dyspepsia, coeliac disease)[13][14][15][16]
Non-gastrointestinal disorders associated with delayed gastric emptying (e.g., eating disorders such as anorexia, neurological disorders such as Parkinson's disease)[17][18][19]
Collagen vascular disorders (e.g., scleroderma, systemic lupus erythematosus, amyloidosis)[20][21][22][23][24]
Endocrine and metabolic disorders (e.g., thyroid dysfunction)[25][26]
Gastric infection (e.g., acute viral infection with varicella zoster, Epstein-Barr virus, cytomegalovirus, rotavirus, and parvovirus-like agents such as Norwalk and Hawaii)[29][30]
Chronic mesenteric ischaemia[31]
Median arcuate ligament syndrome[16]
Alcohol.[34]
Pathophysiology
Normal gastric function is regulated by the complex interaction between the neurohormonal, myoelectric, and contractile properties of the stomach.[35] Receiving ingested foods, mixing them, and emptying nutrients into the small bowel is the most essential motor function of the stomach.[36]
Gastric contractility is thought to be controlled by the gastric slow waves arising from the interstitial cells of Cajal (ICCs) at approximately 3 cycles a minute.[37] The electrical activity generated by the ICCs begins at the junction of the fundus and the body of the stomach, and is conducted circumferentially and distally towards the pylorus. ICCs are linked to the gastric smooth muscle cells, and whenever there is postprandial stimulation of the stomach, electromechanical coupling generates an action potential producing gastric contractility, which results in gastric emptying. This response is also modulated by intestinal peptides such as motilin and cholecystokinin, as well as the vagal nerve. Any process that disrupts the timing or strength of normal gastric contractility results in gastroparesis.
The pathogenesis of diabetic gastroparesis has been well studied. Delayed gastric emptying is thought to be a manifestation of diabetic autonomic neuropathy affecting the vagal nerve, resulting in reduced frequency of antral contractions, decreased gastric tone, lack of antroduodenal co-ordination, antral hypomotility, and pylorospasm, leading to slow emptying of solids.[20][38][39][40] Some evidence also suggests that disruption of the ICC network, direct glucose toxicity, and impaired postprandial release of gastrointestinal hormones in people with diabetes predispose them to gastroparesis.[41][42][43][44]
The role of the vagal nerve in normal gastric emptying is emphasised by the fact that inadvertent vagal nerve injury during procedures such as fundoplication, or demyelination of the vagal nerve nuclei due to disease processes such as multiple sclerosis, cause gastroparesis.[6][45][46]
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